Pheophorbide A isolated from Gelidium amansii inhibits adipogenesis by regulating adipogenic transcription factors and AMPK in 3T3-L1 adipocytes

Adipocyte lipid accumulation causes adipocyte hypertrophy and adipose tissue increment, leading to obesity. As part of our efforts to isolate antiobesity agents from natural prod-ucts, we first isolated the active compound from the extract of Gelidium amansii through bioassay-guided fractionation. We then hypothesized that pheophorbide A isolated from G amansii inhibits adipogenesis by downregulating adipogenic transcription factors; therefore, the antiadipogenic effects of pheophorbide A were investigated in 3T3-L1 adipocytes. On dif-ferentiation of 3T3-L1 preadipocytes into adipocytes, they were treated with pheophorbide A (0-83 mu M). Pheophorbide A inhibited triglyceride accumulation (half maximal inhibitory concentration = 114.2 mu M) and stimulated glycerol release in a dose-dependent manner in 3T3-L1 adipocytes. In addition, pheophorbide A significantly decreased leptin concentra-tions in 3T3-L1 adipocytes. Pheophorbide A inhibited adipogenesis by suppressing the ex-pression of adipogenic transcriptional factors including peroxisome proliferator-activated receptor gamma, CCATT/enhancer binding protein alpha, sterol regulatory element binding protein 1c, and fatty acid synthase. It also induced the expression of phosphorylation of AMP-activated protein kinase. Therefore, these results suggest that pheophorbide A may be useful for pre-venting or treating obesity because of its inhibitory effect on adipogenesis.(c) 2022 Elsevier Inc. All rights reserved.

Automated summary

A compound called pheophorbide A, isolated from Gelidium amansii, has been found to inhibit adipogenesis and may be useful in preventing obesity.